小柯机器人

美国罗彻斯特大学Vera Gorbunova、Andrei Seluanov小等研究人员合作发现，昼夜节律和多能性网络是长寿调节的两大支柱。这一研究成果于2022年5月16日在线发表在国际学术期刊《细胞—代谢》上。

研究人员对具有不同寿命的26个物种进行了比较性的转录组学研究。研究人员发现有数千个基因的表达水平与物种的最大寿命呈负相关或正相关（Neg- 或 Pos-MLS基因）。Neg-MLS基因主要参与能量代谢和炎症。Pos-MLS基因在DNA修复、微管组织和RNA运输方面显示出丰富的内容。Neg-和Pos-MLS基因的表达受到干预措施的调节，包括mTOR和PI3K的抑制。

调控网络分析显示，Neg-MLS基因受到昼夜节律的调节，可能是为了避免持续的高表达，而Pos-MLS基因是核心多能性调节因子OCT4和NANOG的靶标，并在体细胞重编程期间被上调。Pos-MLS基因在胚胎发育过程中高度表达，但在出生后明显下调。这项工作通过定义与整个哺乳动物的长寿相关的途径，并发现昼夜节律和多能性网络是长寿的核心调节因子，为抗衰老干预提供了目标。

据介绍，哺乳动物的最大寿命有100多倍的差异。

附：英文原文

Title: Comparative transcriptomics reveals circadian and pluripotency networks as two pillars of longevity regulation

Author: J. Yuyang Lu, Matthew Simon, Yang Zhao, Julia Ablaeva, Nancy Corson, Yongwook Choi, KayLene Y.H. Yamada, Nicholas J. Schork, Wendy R. Hood, Geoffrey E. Hill, Richard A. Miller, Andrei Seluanov, Vera Gorbunova

Issue&Volume: 2022-05-16

Abstract: Mammals differ more than 100-fold in maximum lifespan. Here, we conducted comparativetranscriptomics on 26 species with diverse lifespans. We identified thousands of geneswith expression levels negatively or positively correlated with a species’ maximumlifespan (Neg- or Pos-MLS genes). Neg-MLS genes are primarily involved in energy metabolismand inflammation. Pos-MLS genes show enrichment in DNA repair, microtubule organization,and RNA transport. Expression of Neg- and Pos-MLS genes is modulated by interventions,including mTOR and PI3K inhibition. Regulatory networks analysis showed that Neg-MLSgenes are under circadian regulation possibly to avoid persistent high expression,whereas Pos-MLS genes are targets of master pluripotency regulators OCT4 and NANOGand are upregulated during somatic cell reprogramming. Pos-MLS genes are highly expressedduring embryogenesis but significantly downregulated after birth. This work providestargets for anti-aging interventions by defining pathways correlating with longevityacross mammals and uncovering circadian and pluripotency networks as central regulatorsof longevity.

DOI: 10.1016/j.cmet.2022.04.011

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00138-3

Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
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